HISTOPATHOLOGY AND PATHOPHYSIOLOGY OF SECONDARY HYPERPARATHYROIDISM DUE TO CHRONIC-RENAL-FAILURE

Between 1973 and 1992, 300 patients underwent parathyroidectomy for se condary hyperparathyroidism due to chronic renal failure in our depart ments. Using parathyroid glands obtained at operation, histopathologic al studies were performed, and to estimate pathophysiology DNA analysi s of parathyroid cell nuclei and calcium-regulated parathyroid hormone (PTH) secretion in vitro were estimated. PTH mRNA expression was eval uated by in situ hybridization. The typical histopathological findings were asymmetric enlargement, nodularities and increased number of oxy phil cells. Secondary hyperplasia was divided into 2 types: diffuse an d nodular type hyperplasia. In the histopathological study nodular hyp erplasia indicated more aggressive proliferation. In DNA analysis the relative number of scattered cells in the DNA synthesis phase was sign ificantly greater in nodular than in diffuse hyperplasia. The half of the maximal inhibition of PTH secretion for calcium (the set-point) in the cells from nodular hyperplasia was higher than in the cells obtai ned from diffuse hyperplasia. However, there was no difference in expr ession of PTH mRNA in nodular and diffuse hyperplasia. These data sugg ested that nodular hyperplasia was more progressively hyperplastic, ha d more aggressive proliferative activities and showed more abnormal re gulation of PTH secretion. These results imply that to prevent graft-d ependent recurrent hyperparathyroidism after parathyroidectomy, the no dular hyperplastic tissue should not be autografted.